Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

F. László, B. J R Whittle

Research output: Contribution to journalArticle

Abstract

The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with L-arginine (300 mg/kg s.c.) 15 min prior to L-NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor-receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01- 0.2 μg/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.

Original languageEnglish
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume13
Issue numberSUPPL. NOV.
Publication statusPublished - 1998

Fingerprint

NG-Nitroarginine Methyl Ester
Jejunum
Vasopressins
Indomethacin
Nitric Oxide
Capillary Permeability
Nitric Oxide Synthase
Serum Albumin
Arginine
Wounds and Injuries

Keywords

  • Indomethacin
  • Intestinal inflammation
  • N(G)-nitro-L-arginine methyl ester
  • Nitric oxide
  • Plasma leakage
  • Vasopressin
  • Vasopressin receptor antagonist

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

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abstract = "The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with L-arginine (300 mg/kg s.c.) 15 min prior to L-NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor-receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01- 0.2 μg/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.",
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T1 - Early phase microvascular interactions in rat jejunum between nitric oxide and vasopressin following indomethacin administration

AU - László, F.

AU - Whittle, B. J R

PY - 1998

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N2 - The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with L-arginine (300 mg/kg s.c.) 15 min prior to L-NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor-receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01- 0.2 μg/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.

AB - The involvement of endogenous vasopressin in the actions of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability after 1 h, as determined by the leakage of radiolabelled serum albumin. In contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.), significant dose-dependent plasma leakage occurred in the jejunum. Pretreatment with L-arginine (300 mg/kg s.c.) 15 min prior to L-NAME prevented these changes in microvascular permeability. Moreover, pretreatment with the vasopressin pressor-receptor antagonist, d(CH2)5Tyr(Me)AVP (0.01- 0.2 μg/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving vasopressin in the rat jejunum. This suggests a protective role of NO, formed by constitutive NO synthase, counteracting effectively the deleterious actions of endogenous vasopressin.

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